Abstract

We investigated the effects of cortical devascularization on the proliferation, differentiation, and migration of neural stem cells (NSCs) in the subventricular zone (SVZ) of the lateral ventricle of adult rats. 60 adult male Wistar rats were randomly divided into control group and devascularized group. At 15 and 30 days after cerebral cortices were devascularized, rats were euthanized and immunohistochemical analysis was performed. The number of PCNA-, Vimentin-, and GFAP-positive cells in the bilateral SVZ of the lateral wall and the superior wall of the lateral ventricles of 15- and 30-day devascularized groups increased significantly compared with the control group (P < 0.05 and P < 0.01). The area density of PCNA-, Vimentin-, and GFAP-positive cells in cortical lesions of 15- and 30-day devascularized groups increased significantly compared with the control group (P < 0.05 and P < 0.01). PCNA-, GFAP-, and Vimentin-positive cells in the SVZ migrated through the rostral migratory stream (RMS), and PCNA-, GFAP-, and Vimentin-positive cells from both the ipsilateral and contralateral dorsolateral SVZ (dl-SVZ) migrated into the corpus callosum (CC) and accumulated, forming a migratory pathway within the CC to the lesioned site. Our study suggested that cortical devascularization induced proliferation, glia-directed differentiation, and migration of NSCs from the SVZ through the RMS or directly to the corpus callosum and finally migrating radially to cortical lesions. This may play a significant role in neural repair.

Highlights

  • Cerebral ischemic stroke is a leading cause of human death and disability [1,2,3]

  • PCNA, GFAP, and Vimentin-positive cells were mainly distributed in the lateral wall of the anterior corner of the lateral ventricle, especially in the dorsal wall of the lateral ventricle

  • Studies found that acute injury can promote the proliferation of neural stem cells (NSCs) in the subventricular zone (SVZ) such as stroke [17, 18], brain injury [19, 20], and neurodegenerative diseases like Alzheimer’s disease [21, 22], Parkinson’s disease [23, 24], and experimental autoimmune encephalomyelitis (EAE) [25,26,27,28] or epilepsy [29]

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Summary

Introduction

Cerebral ischemic stroke is a leading cause of human death and disability [1,2,3]. Stroke and traumatic brain injury lead to cell death, characterized by a loss of neurons and glial cells within the brain [4, 5]. In the early 1990s, self-replicating neural stem cells (NSCs) were identified in the central nervous system (CNS) These cells proliferate, migrate, and differentiate into all the cell types of the brain and spinal cord, including neurons, astrocytes, and oligodendrocytes [6,7,8]. NSCs in a resting state activate, proliferate, migrate to the injured site, and differentiate into new nerve cells. These new cells can replace injured cells, participate in the formation of new neural circuits, and promote the structural and functional repair of the brain damage [15]

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